NMDA-NR1 receptor subunit mRNA expression in rat brain after 6-OH-dopamine induced lesions: A non-isotopic in situ hybridization study

Andrés, Marı́a Estela; Gysling, Katia; Araneda, Silvia; Venegas, Angela; Bustos, Gonzalo

doi:10.1002/(sici)1097-4547(19961101)46:3<375::aid-jnr11>3.0.co;2-0

Cited by 22 publications

(4 citation statements)

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“…1997). It is worth noting that Andres et al . (1996) reported a striking increase in NMDA receptor 1 mRNA signals in the striatum but not in the cerebral cortex after 6‐OHDA injection in the adult rat.…”

Section: Discussionmentioning

confidence: 99%

“…Although we measured SMA with the inclusion of all kinds of behavior, alteration in the levels of expression of NMDA receptors may also reflect other behavioral abnormalities, such as self-mutilation (Moy et al 1997). It is worth noting that Andres et al (1996) reported a striking increase in NMDA receptor 1 mRNA signals in the striatum but not in the cerebral cortex after 6-OHDA injection in the adult rat. Results are expressed as in Table 2.…”

Section: Discussionmentioning

confidence: 99%

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Motor activity and gene expression in rats with neonatal 6‐hydroxydopamine lesions

Masuo

Ishido

Morita

et al. 2004

Journal of Neurochemistry

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A rat model of a hyperkinetic disorder was used to investigate the mechanisms underlying motor hyperactivity. Rats received an intracisternal injection of 6-hydroxydopamine on post-natal day 5. At 4 weeks of age, the animals showed significant motor hyperactivity during the dark phase, which was attenuated by methamphetamine injection. Gene expression profiling was carried out in the striatum and midbrain using a DNA macroarray. In the striatum at 4 weeks, there was increased gene expression of the NMDA receptor 1 and tachykinins, and decreased expression of a GABA transporter. At 8 weeks, expression of the NMDA receptor 1 in the striatum was attenuated, with enhanced expression of the glial glutamate/ aspartate transporter. In the midbrain, a number of genes, including the GABA transporter gene, showed decreased expression at 4 weeks. At 8 weeks, gene expression was augmented for the dopamine transporter, D4 receptor, and several genes encoding peptides, such as tachykinins and their receptors. These results suggest that in the striatum the neurotransmitters glutamate, GABA and tachykinin may play crucial roles in motor hyperactivity during the juvenile period. Several classes of neurotransmitters, including dopamine and peptides, may be involved in compensatory mechanisms during early adulthood. These data may prompt further neurochemical investigations in hyperkinetic disorders. Keywords: attention-deficit hyperactivity disorder, DNA array, GABA, 6-hydroxydopamine, NMDA, tachykinin. Pervasive developmental disorders, such as autism and attention-deficit hyperactivity disorder (ADHD), are serious developmental disorders. Patients with these disorders display hyperactivity in inappropriate settings. This hyperactivity, known as hyperkinesia, is particularly frequent in childhood. However, many patients still have difficulties well into adulthood, particularly with communication skills. These disorders can give rise to severely antisocial behavior. The etiology underlying these developmental disorders is not yet clear. However, treatment with psychostimulant drugs, such as methamphetamine or methylphenidate, often attenuates the hyperactivity (Dresel et al. 2000). This suggests that an abnormality in the development of dopamine (DA) neurons may underlie hyperactivity.In order to understand the mechanisms involved in behavioral hyperactivity, several animal models have been used (Viggiano et al. 2003): (i) rats with neonatal lesions of the central DA system induced by the neurotoxin, 6-hydroxydopamine (6-OHDA); (ii) the spontaneously hypertensive rat, Naples high-excitability rat, and congenic wiggling rat; (iii) neonatal rats infected with the Borna disease virus; (iv) genetic knockout mice lacking a functional

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Motor activity and gene expression in rats with neonatal 6‐hydroxydopamine lesions

Masuo

Ishido

Morita

et al. 2004

Journal of Neurochemistry

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“…The observed decrease in nNOS activity does not stem from loss of nNOS colocalized with TH as neither we, nor colleagues (Johnson & Ma 1993; Fujiyama & Masuko 1996), found evidence for such a colocalization. Compensatory responses in the caudate putamen after 6‐OHDA lesions, such as increased NMDA‐NR1 receptor subunit expression (Andrés et al . 1996) and a serotonergic hyperinnervation (Guerra et al .…”

Section: Discussionmentioning

confidence: 99%

NO‐mediated cGMP synthesis in cholinergic neurons in the rat forebrain: effects of lesioning dopaminergic or serotonergic pathways on nNOS and cGMP synthesis

Vente

Ittersum

Abeelen

et al. 2000

Eur J of Neuroscience

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Nitric oxide synthase (NOS) activity and NO-mediated cGMP synthesis were studied in the rat forebrain of control animals and animals which had received a unilateral lesioning of dopaminergic or serotonergic pathways. Lesioning of the dopaminergic innervation using 6-hydroxydopamine resulted in a 50% decrease in NOS activity in the lesioned frontal cortex and caudate putamen. Lesioning of the serotonergic innervation using 5,7-dihydroxytryptamine had no effect on NOS activity. NO-mediated cGMP accumulation in rat forebrain slices was not affected by 6-hydroxydopamine or 5,7, -dihydroxytryptamine lesioning. Using cGMP immunocytochemistry, it was demonstrated that NO-mediated cGMP synthesis was absent from dopaminergic, serotonergic, GABA-ergic and neuronal NOS-containing nerve fibres. A minor colocalization of cGMP immunoreactivity was found in parvalbumin-containing fibres in the cortex. Extensive colocalization between cGMP immunoreactivity and the acetylcholine transporter was found in all cortical areas and in the caudate putamen. There was no effect of the lesions on this colocalization. These results demonstrate NO-mediated cGMP accumulation in cholinergic fibres in the forebrain of the rat and suggest an anterograde signalling function of NO in cholinergic neuronal systems in the cortex and caudate putamen of the rat.

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“…The expression of NMDAR1, NMDAR2A and NMDAR2B mRNA have been also studied in rat striatum a few weeks after 6‐hydroxydopamine (6‐OHDA) lesions of the dopaminergic nigrostriatal pathway, with conflicting results reporting either increases in the NMDAR1 subunit (Tremblay et al ., 1995; Andres et al ., 1996) and NMDAR2A subunit (Ulas & Cotman, 1996) or no changes at all (Rodriguez‐Puertas et al ., 1999). Furthermore, statistically significant decreases of [ 3 H]MK‐801 binding in the striatum of 3‐month‐old weaver mice have been reported recently (Reader & Senecal, 2001).…”

Section: Discussionmentioning

confidence: 99%

Differential effect of dopamine deficiency on the expression of NMDA receptor subunits in the weaver mouse brain

Fragioudaki

Kouvelas

Mitsacos

2003

Eur J of Neuroscience

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The weaver mutant mouse is characterized by degeneration of the dopaminergic mesencephalic neurons. The role of the dopaminergic system in the regulation of N-methyl-d-aspartate (NMDA) receptor subunit expression was addressed in the present study. In situ hybridization experiments were conducted to determine the expression levels of the NMDA receptor subunit mRNAs, z1, epsilon1 and epsilon2, in striatum, nucleus accumbens, olfactory tubercle and cerebral cortical regions of 26-day-, 3- and 6-month-old weaver mice. Data indicated statistically significant increases in z1 and epsilon2 mRNA levels in 6-month-old weaver striatum, whereas at the same age epsilon1 mRNA expression was decreased in all striatal regions, as well as in the cortex. In the 26-day-old weaver striatum and nucleus accumbens, statistically significant increases were observed in epsilon1 mRNA levels, whereas no changes were observed in the other two subunits. In the somatosensory cortex of 26-day-old weaver brain an increased expression of all three subunits was observed. The upregulation of NMDA receptor subunit expression observed in the somatosensory cortex can be attributed to a decreased activity of the glutamatergic thalamocortical pathway, following the degeneration of the nigrostriatal dopaminergic fibres. In the striatum, the present results demonstrate a differential control on the expression of z1 and epsilon2 subunits on the one hand, and epsilon1 subunit on the other. It is suggested that dopamine exerts a negative control on the expression of z1 and epsilon2 subunits, through a downregulation of transcription factors associated with the AP1 regulatory site, which is mediated by the activation of striatal dopamine D2 receptors.

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NMDA-NR1 receptor subunit mRNA expression in rat brain after 6-OH-dopamine induced lesions: A non-isotopic in situ hybridization study

Cited by 22 publications

References 80 publications

Motor activity and gene expression in rats with neonatal 6‐hydroxydopamine lesions

Motor activity and gene expression in rats with neonatal 6‐hydroxydopamine lesions

NO‐mediated cGMP synthesis in cholinergic neurons in the rat forebrain: effects of lesioning dopaminergic or serotonergic pathways on nNOS and cGMP synthesis

Differential effect of dopamine deficiency on the expression of NMDA receptor subunits in the weaver mouse brain

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